Beryllium lung disease is a well-recognized industrial health hazard occurring in both acute and chronic forms. While toxic effects of beryllium are responsible for acute disease, evidence from this and other laboratories supports a role of delayed hypersensitivity (cell-mediated immunity) in the chronic form. Beryllium has also been cited as a carcinogen but data are inconclusive. We have performed extensive clinical and experimental studies of beryllium lung disease and proposed to continue experimental work in characterization of immunopathologic mechanisms. In a previous study, we produced granulomatous lung disease in strain 2 guinea pigs by endotracheal injection of beryllium oxide, and observed both positive skin tests and in vitro lymphocyte blastogenesis to beryllium salts. In addition, the disease was diminished by tolerization or treatment with immunosuppressive drugs. Our major objective in this project will be to examine the effects of experimental beryllium disease on pulmonary macrophage function: an area for which no data are yet available. Pulmonary macrophages obtained by lavage from strains 2 and 13 guinea pigs, receiving endotracheal beryllium injections, will be evaluated with respect to chemotaxis, phagocytosis, cytotoxicity directed against autologous alveolar cells or fibroblasts (autoimmune reactions), bactericidal activity and secretion of elastase, plasminogen activator, lactate dehydrogenase, and beta-glucuronidase. Strain 13, unlike strain 2, animals have been shown not to develop delayed hypersensitivity to beryllium salts. Secondly, we will attempt to determine if immunoglobulin or complement components are involved in experimental disease. Lastly, a minor facet of this study will relate to possible carcinogenic effects of beryllium. Histologic sections of lung tissues from strains 2 and 13 animals will be examined for evidence of granulomatous disease and premalignant changes. Data from this study should benefit our understanding of human beryllium lung disease.